Long Story Short:
Deconstruction of the Peripheral Biomechanical Mind
- Discover some reference to SomaSimple (SS) while looking for reference material/evidence for Shirley Sahrmann’s MIS
- Somewhere in SS Forums, there is mention of EIM boards and RE, both of which I have ventured to on occasion only.
- find some interesting stuff on EIM boards re: pain and a whole debate on some skin technique that sounds a lot on the surface like MFR.
- Diane believes she is treating the brain directly by influencing the skin?
- how is this different (in application, not theory) than gentle MFR or Troy’s voo-doo?
- if she is indeed successful, does this have any commonality with eastern medicine?
- look up a thread on SS for Gua Sha (I have used SASTM)--SS folks seems to think that it is unnecessarliy aggressive
- Visit SS Forums and find a nice thread with some PRI guys. Odd that Darko feels that a lack of Ron’s involvement is unexpected, but there are a couple PRI guys willing to take up the cause. Seems that SS peeps want there to be a good theory behind what isi happening and if there is not a neuro component, they will automatically discredit it.
- Be careful in here, they can be very forward...not that there is anything wrong with that, but be ready for it should you take an opposing viewpoint.
- their confrontational stance makes sense if has the intent of inquiry and weeding out bull shit.
- SS peeps point out that if there is a common presentation across the entire population (which I with PRI that it seems it is there), why does it only cause pain in a select population...I feel their frustration, even if I have had some success with it.
PRI: novel movements/motor activities coupled with strong diaphragmatic breathing...does this help in the inhibition that is being referenced in some speeches/threads and thus reduce pain and improve mobility for a different reason than proposed by Hruska (if at all?). It seems that there could be some overlap here...after all, PRI was fascinating to me b/c of the proposed neuro component (breathing, inhibition, activation without direct regard for strength measures per-see).
- included link to Jason's Pain handouts
- included files on neuromobilization by Cory
- included mention of Moseley youtube video: is 40+ min long, but entertaining and a nice primer on some of the stuff that has been referenced the last couple of days.
- describes nicely and in an entertaining way, how pain comes to be (analogies made to visual trickery and his snake story, to illustrate that the brain uses context for output, not just sensory input)
- makes mention of descending inhibition/facilitation for the first time to me: the body telling the spinal cord to stop sending/increase info to the thalamus as there is lesser/greater threat than the cord "thinks"
- this is the first I have heard of the nocioceptive system in the brain becoming "sensitized", requiring less stimulation from the periphery to actualize a potential up to the brain, because the brain has facilitated the activation of the nocioceptors...keep in mind this is not enough in and of itself for chronic pain
- also found a link to this thread by Jason that finishes saying: “The more I practice and think, the LESS CERTAIN I become about everything. I thought that’s how every scientist felt, but the smug certainty shown sometimes by those defending the OMPT paradigm can not be backed up by either the existing data or a spirit of scientific inquiry.”
- Also need to poke my head in here
- ...and the zombiefication of PT
- a link is also provided to the SS bibliography
- DONE REVIEWING WELCOME, BIENVENUE
- Woke up to find that I might have hit a nerve saying that I think that the US medical system should go cash pay...waiting to see what is up with that. Do some oppose a cash model, or did they disagree with my assertion that our difficulties in this country are cultural?
- Turns out there was a big thread that started in 2009 re: US Healthcare reform...some thought that my remarks re: cash pay were going to rekindle some fires, but Diane has greater interest in speaking on the impact of MDs going to a cash pay model and POPs.
- Diane makes reference to this book, titled “The Patient’s Brain”, there is a convo of the book here after others have read it
- Some strong encouragement as to how quickly I will see results from this “new approach to treatment.
- encouraged to obtain Moseley’s Yarns book and to read Dorko’s essays to be able to help patient’s most quickly
- Interesting to see how little respect I get in the clinic due to pt expectation before they walk in the door compared to Nari in Australia
- refers to the anterior cingulate: helps you “feel” being in pain when you imagine pain, or someone you care about. Value is here for good and bad...evolution has jammed psychic pain in the same area as true pain (i.e. callouses)
- this region lights up with patients with clincal depression
- substance P has to do with function here in the anterior cingulate...is associated with anti-depression and pain reflief
- their emotions had developed an accurate sense of fear. They knew which decks were dangerous. In other words, their feelings figured out the game first – the hand was leading the brain.
- Interestingly, neurological patients unable to experience any emotion at all – they have a damaged orbitofrontal cortex – proved incapable of selecting the right cards.
- Geez...have spent about 2 hours parsing and organizing the first of the starter threads I foudn proposed by Caro yesterday
- Cory is the man...I cannot believe how he has synthesized all of the lit her has read, and then typed it out as he has. If this makes sense when I actually read it tomorrow, I will be eternally grateful.
- In this thread featuring Cory, there is a link to an interesting thread re: Self Ideomotion
- the moral of the story is that one need not get necessarily get caught up in the minutiae of what nerve is troublesome
- purchased Explain Pain...will arrive in 2 days (love Amazon Prime!)
- Printed off the word doc I made from all of Jason’s postings in his unified theory thread
- having a hard time getting past the premise from Damasio
- there is some rigorous debate about his theory, esp from Maia and McClellan...how does one keep reading another pages if the premise is so much in question? Has it grown stronger since 2004-5? Would the rest of the theory of practice crumble should this foundational element be misguided?
- Ok, onto the 2nd of Caros recommended intro threads: interesting discussion on changing patient expectation and the role of Placebo...are no specific effects of treatment?
- “…it is clear that input to map representation at various levels may be sufficient to convince the brain that threat has been resolved, eg, CRPS is reduced by both higher level motor input and visual input representation. The existence of placebo would rule out the claim that any aspect of therapy, other than expectation, is necessary, but that doesn't mean that input into the motor representation maps is not sufficient to resolve a discordance (if that is truly the problem).”
- Barrett makes restates the point that just b/c something is not in itself necessary does not mean that it is not sufficient
- a link is here to a thread about causality
- Here on Soma Simple we have a sense of how we’ve arrived; through a jungle full of traps and impediments. Our colleagues have had an easier trip. Across the gentle slopes of mesodermaland they’ve been guided by the programs and fellowships that don’t allow much in the way of dissonance or uncertainty. Traps are easily navigated or ignored - their hands have been held. Ultimately, they get the same positive reactions from a common patient population and can hardly be blamed for thinking and behaving as they do -Barrett
- Diane is stressing the grooming more here than I have read previously...(kinesthetic brain food)
- ....the methods I use reduce my reliance upon luck – they will never eliminate it entirely -Barrett
- I simply remember that placebo is given to us by the patient, not received by them from the therapist -Barrett
- That's on the right track, in terms of where the placebo is coming from. The quote is more along the lines of, "A placebo response is something to be elicited from a patient, not given to them.” -Diane
- Another consideration is this: A patient enters a room which is perceived as threatening in some way, and a nocebo response is elicited. This may persist despite any therapist's methods. -Nari
- I wouldn't disagree with that, but just as context and threat are important to the brain, so is the incoming afferent message. I don't think at this time we can be so certain that placebo is it - certainly the research into NSAID effectiveness for example shows an effect larger than placebo so I'm not sure why we would think that mechanical input would not be an important consideration. I mean, the brain is deciding things there in the presence and then subsequent decrease of a chemical afferent signal, right? -Jason S
- Regarding specific and non-specific effects, perhaps a clearer way of thinking of this is what is necessary in order to bring about the sufficiency of a given treatment approach. -Cory
- Luke references Butler: The suggestion that techniques that cause a painful response are invariably undesired (Greening and Leary, 2006) deserves further consideration. The patient’s condition, the pain mechanism in operation and the patient’s understanding of the pain may be such that a (mildly) painful response during, or for a short duration after activity or techniques, may not be problematic and may be the most optimal path to recovery.
- Diane provides a link of an article in Journal of Family Medicine that addresses placebo vs placebo response as well as an article by Benedetti
- Karen suggests a few starting points here as well
- Barrett started a thread titled 5-questions in 2006, of course it is 4 pages long
- Bedtime with more things to read and less time to read them...was happy to have listened to a nice addiction podcast and am in the middle of a Damasio podcast that speaks to Emotions and Feelings, how emotions are important for survival and how feelings help us understand a context from our emotions and experiences...something that we can learn from.
- Feeling like I am over my head and am unable to navigate the waters without capsizing...was hoping the unified theory thread was going to helpful...maybe not?...no, it has to be. Maybe I can PM someone to ask them about Damasio and Maia?
- Nah...made a posting in my welcome thread instead
- No real reading today, just a realization in the am that being a sponge is no longer good enough, especially after someone else’s sieve/strainer
- Came to have a wonderful understanding of Somatic Marker Theory this am when thinking of the car accident I avoided this past winter...there were 36 possible actions and only chose between 2.
- accel, brake, e-brake, nothing
- left, right, nothing (after L, do I stay on the road or go off)
- shift down, do nothing
- differentiates that social and acquired SCRs (images with social context: people they know, horrific suffering) are impacted by the ventromedial pre-frontal region while unaquired SCRs (noise, light) are not...despite a conscious knowledge of these people/events
- other studies with people who have injuries in other areas may impact the brain’s ability to bring knowledge to a conscious level, but they have SCRs that show an innate knowledge of people/stimuli (good/bad)
- Found a nice critique of SMT online as well
- Looking fwd to receiving Explain Pain tomorrow.
- Nice PPT presentation on pain in this thread
- PT is helpful with true lesions of connective tissue (i.e. sprain, postop)
- Clearly, many of our patients have connective tissue injuries and problems that respond predictably to stress, movement, strengthening, and rehabilitation. Our profession is rather expert at helping these people and improving their function. Also, just as clearly, there are segments of our patient population whose symptoms cannot adequately be explained by a physical injury, loss of ROM or strength, problems with muscle length, or many of the other biomechanical measures that we have been taught are so important. Clearly, these patients seem to require a different approach, and we ignore that fact and the foundational science that supports it at our peril. We need both a connective tissue and a neural tissue (or mesodermal vs ectodermal) approach if we are to be successful for a wide variety of patients.
- If the manual examination process was found to lack reliability or validity, that would be a very serious blow to the foundation of orthopedic manual therapy. In other words, if it was difficult for therapists to agree about the “findings” of the examination both between and within therapists (inter and intra-rater reliability) or the manual exam findings were not capable of discriminating between those with and without pain (a measure of validity) then a most serious problem will have been revealed. Would it surprise anyone to learn that the reliability (both inter- and intra-) of most manual examination procedures is quite poor? Would it surprise anyone to learn there have precious few studies looking at the presence or absence of these findings in an asymptomatic population?
- Again, we see major flaws [measures of strength, ROM, joint mobility, etc]. There have been very few studies attempting to assess the presence of these impairments in asymptomatic vs symptomatic patients. Studies demonstrating resolution of these impairments are unable to draw a conclusive causal relation between impairment and complaint, and there are many studies showing resolution of complaint after treatment even when one or more impairment(s) remain. Clearly, we cannot think too highly of these impairments as indicative of a superior treatment model, the evidence just isn’t there yet.
- There has been no causal link between static posture and pain, and many complaints for which our patients seek assistance cannot be demonstrated on imaging studies designed to assess the health of these tissues. Multiple studies have demonstrated no causal link whatsoever between degeneration of connective tissue and the presence of pain and function complaints. Clearly, focusing on connective tissue alone is a flawed paradigm.
- Often the recent LBP CPR for manipulation is mentioned in an apparent attempt to bolster points about the value of the OMPT paradigm. Unfortunately, the findings of the manipulation CPR for LBP do much more to refute the OMPT paradigm then they support it.
- These studies conclusively proved that many of the detailed examination procedures we were using to determine likely success with manipulation were completely incorrect and actually useless! The two measures of impairment (generalized PA mobility and hip rotation ROM) were not very specific, nor all that reliable between therapists.
- Some impairment measures appear to be very useful in selecting appropriate treatment (such as lumbar PA mobility) and there is little doubt that for connective tissue injuries, skill in a manual examination and clinical reasoning process is critical. To the degree the OMPT paradigm does that, it will achieve (and has achieved) success. However, there are large numbers of patients whose primary complaint of pain cannot be traced to dysfunction in the strength, mobility, or joint kinematics of a connective tissue structure or structures. These patients will continue to *not improve* with traditional OMPT care, because that paradigm is not designed to examine or treat non-connective tissue structures.
- You call them "models" and that might be accurate, but though a model may be accurate, it isn't necassarily relevant. Theories, on the other hand, possess relative degrees of accuracy, ostensibly improving as evidence becomes available. The orthopedic model used to drive coercive management for painful problems cannot be successfully defended when placed in relation to the neurobiology forming the basis of the methods you recently learned. What you've learned, I think, is a new perspective. Orthopedics (mesoderm) is inextricably linked (@@@@@@) to the ectoderm, but is insufficient to explain much. -Barrett
- I also got through the “F word” thread...a mostly semantical thread IMO (maybe I will change my position later (?) regarding the over-utlization of the the term function/functional...but coming from my peds background, maybe I see things from a different context.
- loved Cory’s thought though: I think my problem is that the term when used appropriately really should be stated as "contextually relevant." But functional, as it is used, implies other things
- this is how I think of function, but suppose people are seeing it used in other contexts and are therefore taking umbrage.
- AH HA---I think they are referencing Gary Cook...FMS...now this makes sense to me and I am now in agreement.
- Ron links to a RE posting of his that had a nice thought: We were built for intermittent physical stress and this is how I put it to the patient. I've tossed "no pain no gain" and now use "no effort no adaptation" or "no stress no adaptation".
- Reading Explain Pain....
- there was reference to epicondylitis in Explain Pain...got me thinking nerve vs meso:
- The purpose of this study was to investigate the treatment response in lateral epicondylitis (tennis elbow) by MRI. Magnetic resonance imaging was obtained in 30 patients with clinical symptoms of lateral epicondylitis of the elbow using T1-, T2- and T2-weighted fat-saturated (FS) sequences. The patients were randomised to either i.m. corticosteroid injection (n=16) or immobilisation in a wrist splint (n=14). Magnetic resonance imaging of the elbow was performed on a 1.5-T MR system at baseline and after 6 weeks. The extensor carpi radialis (ECRB) tendon, the radial collateral ligament, lateral humerus epicondyle at tendon insertion site, joint fluid and signal intensity changes within brachio-radialis and anconeus muscles were evaluated on the MR units workstation before and after 6 weeks of treatment. The MRI was performed once in 22 healthy controls for comparison and all images evaluated by an investigator blinded to the clinical status of the subjects. The MR images showed thickening with separation of the ECRB tendon from the radial collateral ligament and abnormal signal change in 25 of the 30 patients on the T1-weighted sequences at inclusion. The signal intensity of the ECRB tendon was increased in 24 of the 30 patients with lateral epicondylitis of the elbow on the T2-weighted FS sequences. In the patients there were no associations between pathologically signal intensity within the ECRB tendon on T1- and T2-weighted sequences and the degree of self-reported pain (Dumbells test) at inclusion. In general, the MRI changes persisted in the patients at follow-up after 6 weeks despite clinical remission. The increased signal intensity within the extensor tendon is indicative of lateral epicondylitis humeri. The changes in signal intensity and morphology of ECRB tendon seem to be chronic and may persist despite clinical improvement.
- Background: Medial epicondylitis, or golfer’s/pitcher’s elbow, develops as a result of medial stress overload on the flexor muscles at the elbow and presents as pain at the medial epicondyle. Cervical radiculopathy has been associated with lateral epicondylitis, but few associations between the cervical spine and medial epicondylitis have been made. Researchers propose that there is an association, suggesting that the weakness and imbalance in the elbow flexor and extensor muscles from C6 and C7 radiculopathy allow for easy onset of medial epicondylitis....Hypothesis: Medial epicondylitis will present in over half the patients diagnosed with C6 and C7 radiculopathy....Methodology: A total of 102 patients initially presenting with upper extremity or neck symptoms were diagnosed with cervical radiculopathy. They were then examined for medial epicondylitis. Data were collected by referring to patient charts from February 2008 until June 2009. ….Results: Fifty-five patients were diagnosed with medial epicondylitis. Of these, 44 had C6 and C7 radiculopathy whereas 11 presented with just C6 radiculopathy.....Conclusion: Medial epicondylitis presented with cervical radiculopathy in slightly more than half the patients. Weakening of the flexor carpi radialis and pronator teres and imbalance of the flexor and extensor muscles from the C6 and C7 radiculopathy allow for easy onset of medial epicondylitis. Patients with medial epicondylitis should be examined for C6 and C7 radiculopathy to ensure proper treatment. Physicians dealing with golfers, pitchers, or other patients with medial epicondylitis should be aware of the association between these 2 diagnoses to optimize care.
- Objective: To compare the MR imaging findings of 13 patients with clinically diagnosed medial epicondylitis with the MR imaging findings of 26 patients of similar age with no clinical evidence of medial epicondylitis....Design and Patients: The study group consisted of 13 patients with clinically diagnosed medial epicondylitis. The control group consisted of 26 patients of similar age with no clinical evidence of medial epicondylitis. The medical records and MR imaging findings of these patients were retrospectively reviewed by two fellowship-trained musculoskeletal radiologists....Results: Eleven of the 13 patients in the study group had thickening and increased signal intensity of the common flexor tendon on both T1-weighted and T2-weighted images. The remaining two patients in the study group had soft tissue edema around a normal-appearing common flexor tendon. Twenty-one of the 26 patients in the control group had a normal-appearing common flexor tendon on MR imaging. Three patients in the control group had a thickened common flexor tendon which was of intermediate signal intensity on T1-weighted images but of uniform low signal intensity on T2-weighted images. Two patients in the control group had a thickened common flexor tendon which was of intermediate signal intensity on both T1-weighted and T2-weighted images. None of the patients in the control group had soft tissue edema around the common flexor tendon.....Conclusion: MR imaging findings of patients with clinically diagnosed medial epicondylitis included thickening and increased T1 and T2 signal intensity of the common flexor tendon and soft tissue edema around the common flexor tendon. The presence of intermediate to high T2 signal intensity or high T2 signal intensity within the common flexor tendon and the presence of paratendinous soft tissue edema were the most specific findings of medial epicondylitis on MR imaging.
- Conclusion: The CEO is confirmed as the primary site of MRI changes in tennis elbow. Oedema was commonly found in asymptomatic elbows, necessitating the presence of thickening or tears in the CEO tendon to objectively diagnose tennis elbow on MRI.
- Finished Explain Pain...gotta move on now to something else. Order Wall’s Pain and Damasio’s Descarte’s Error...both are cheap and in paperback
- am gonna hold off on NOI/Shacklock stuff until I understand pain better
- back to the boards tomorrow.